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Tim's Cards > Endocrinology III > Flashcards

Endocrinology III Flashcards

1
Q

Where does Insulin act?

A

Muscle and fat

GLUT4 transporters

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2
Q

T/F

Insulin inhibits lipolysis

A

True

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3
Q

What becomes dominant when insulin decreases?

A

Glucagon - liver

Epinepherine - muscle

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4
Q

Why can’t insulin be given orally?

A

Peptide hormone

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5
Q

Type I diabetes is due to insulin _______.

Type II diabetes is due to insulin _______.

A

Deficiency

Resistance

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6
Q

What 3 requirements are there for a random plasma glucose Diabetes diagnosis?

A

Glucose > 200 mg/dl
polyuria
polydipsia

(and/or weight loss)

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7
Q

Why is there still high blood glucose in a diabetic in the fasting state?

A

There’s not enough insulin to get glucose from GNG and glycogenolysis into the cell.

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8
Q

Hemoglobin A1c glucose level above _____ suggests diabetes.

A

6.5%

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9
Q

T/F

Pre-diabetes always progresses to diabetes.

A

False

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10
Q

Define:
polyuria
polydipsia
polyphagia

A

(excessive)
urination
thirst
food intake

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11
Q

What contributes to diabetic hyperglycemia in the intestine and the kidney?

A

Intestine: decreases GLP-1
Kidney: SGLT-2 (glc transporter) over-expressed

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12
Q

What are some tests to confirm Type I diabetes?

A

GAD (glutamic acid decarboxylase antibody)

ICA (islet cell cytoplasmic autoantibodies)

*GAD long-lasting

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13
Q

There are many environmental factors leading to Type II diabetes. What are the 2 most important?

A

Obesity

Aging

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14
Q

What most often breaks in type II Diabetes?

A

Post-receptor actions

pre-receptor is rare and receptor defects not often

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15
Q

Ketones suggest…

A

Type I

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16
Q

What is a non-insulin treatment for Type II diabetes that decreases liver glc production and fasting glc?

A

Biguanide

metformin

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17
Q

What is an effective therapy for diabetes that stimulates beta cells, inhibits alpha cells, and decreases appetite?

A

Incretins

GLP-1

*expensive and effective

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18
Q

What do SGL2T2 inhibitors do?

A

inhibit excretion of glc

*newest drugs

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19
Q

What are the 2 background insulins?

long lasting, no peak

A

Glargine and Detemir

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20
Q

What does it mean if blood glucose is high before a meal in a diabetic?

A

The previous meal wasn’t covered enough by insulin

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21
Q

What can too much insulin cause?

A

Hypoglycemia
loss of consciousness
death

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22
Q

What are 2 hormonal causes of hypoglycemia?

A

GH or Cortisol deficiency

*these cause insulin resistance. With no insulin resistance, glucose is taken up by muscle and fat and not enough for the brain

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23
Q

What is a better treatment than snickers for hypoglycemia?

A

Glucagon injection

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24
Q

What leads to lipolysis in type I diabetes?

A

unopposed Glucagon

*ketoacidosis

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25
Q

What enzyme, suppressed by insulin, is over-active in response to epinephrine in type I diabetics?

A

Hormone Sensitive Lipase

*fat pours out of adipose tissue=ketoacidosis

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26
Q

Why does ketoacidosis not occur in Type 2 diabetes?

A

insulin deficient but not completely absent

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27
Q

What does high blood glucose, high urine glucose, and salt/water loss lead to?

A

Dehydration and High Serum Osmolality

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28
Q

What happens to tissues freely permeable to glucose in long-term diabetes?

A

They break down

Microangiopathies (retinopathy, neuropathy, nephropathy)
Macroangiopathy (cerebral, coronary, peripheral)

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29
Q

What are AGE’s?

A

Advanced Glycation Endproducts

*highly reactive consequence of too much glc
free radicals , cross linked proteins, etc.

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30
Q

What is ischemia?

A

Low oxygen to tissues

consequence of chronic hyperglycemia

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31
Q

What reduces inflammation in treatment for diabetic retinopathy?

A

Glucocorticoid

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32
Q

What risk factor goes way up in diabetic nephropathy?

A

heart disease

mortality 20-40 times higher

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33
Q

What is the mechanism of the slowed neural conduction in diabetic neuropathy?

A

semental demyelination

*distal first - which is why problems with feet

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34
Q

What are the conditions that comprise metabolic syndrome?

need 3 of these

A 
Hyperinsulinemia
Hyperglycemia
Hypertriglyceridemia
Low HDL cholesterol
Hypertension
Central obesity
35
Q

What causes foot problems in diabetics?

A

Loss of feeling
Poor blood supply
Poor wound healing

(combined microvascular neuropathy and macrovascular disease)

36
Q

Does intensive treatment of type I diabetes slow the onset of progression of disease?

A

Yes

*bigtime

37
Q

Does intensive glucose control prevent macrovascular complications in Type II diabetes?

A

No.

*macrovascular disease outcomes the same

38
Q

What two factors, if controlled, can benefit type II diabetes?

A

Blood pressure and Lipid control

39
Q

How often should the feet be examined with a Diabetic patient?
What common drug can be useful in preventing other complications?

A

Daily

Aspirin

40
Q

What do Leydig cells do?

A

Produce testosterone in presence of LH

*in testes

41
Q

What is the function of Sertoli cells?

A

secrete mullerian inhibiting substance

“nurse” spermatogenisis process

42
Q

When do gonads differentiate?

A

6 weeks

43
Q

Describe the differentiation process at about 7 weeks.

A

Testosterone stimulates Wolffian ducts

Mullerian inhibiting substance degenerates Female (mullerian) ducts

44
Q

What do the formation of the penis, scrotum, and prostate require?
What enzyme is involved?

A

DHT - dihydrotestosterone

5-alpha-reductase

*undervirillization usually defect in process (usually amount of DHT)

45
Q

review:

Male gonad feedback loops

A

GnRH > LH/FSH > Testosterone

46
Q

What stimulates the testes to make testosterone before and after 12 weeks?

A

Before 12 weeks: HCG (human chorionic gonadotropin) from placenta

After 12 weeks: FSH/LH from fetal pituitary

47
Q

What does micropenis suggest?

A

Fetal pituitary failure

  • low LH = low testosterone = low DHT = micropenis
  • *must screen for other pituitary deficiencies
48
Q

Testosterone effects the development of the ______ genitalia and dihydrotestosterone effects the development of the _____ genitalia.

A

Internal (vas defrens, etc)

External (scrotum, prostate, etc)

49
Q

What does the maintenance of testicular germinal structures depend on?

A

Local testosterone

intra-testicular

50
Q

What hormone stimulates the testes to produce testosterone?

A

LH

51
Q

How are GnRH and LH/FSH secreted?

A

pulses

52
Q

What type of cells are stimulated by LH?
FSH?
(in men)

A

LH - Leydig cells (testosterone)
(this diffuses to Sertoli cells)

FSH - Sertoli cells (Inhibin B)
*androgen binding protein

53
Q

GnRH >

complete feedback

A

LH > Leydig cells > Testosterone

FSH > Sertoli cells > Inhibin

54
Q

What can convert testosterone to estradiol?

A

Aromatase

found mostly in fat

55
Q

What is the abnormal migration of GnRH-producing neurons and (bundled with) olfactory neurons called?

A

Kallman syndrome

*hypogonadism and no sense of smell

56
Q

How are tertiary (hypothalamic) defects in sex hormones treated?

A

At primary level with testosterone

if fertility is the issue requires FSH/LH or GnRH via pump

57
Q

HCG act in place of…

A

LH

58
Q

If there is trouble at the testes what are hormone levels?

A

high GnRH, FSH, LH

low Testosterone

59
Q

If someone is born without testes, what is the external genitalia?

A

female (internal and external)

60
Q

When do testes fail in Klinefelter Syndrome?

A

After puberty

61
Q

What are some target tissue defects in sexual differentiation?

A

Defective androgen receptor, 5-alpha-reductase (no DHT), aromatase (no estrogen)

62
Q

If the testes are present but there are defective androgen receptors what would the hormone levels be?

A

high GnRH, FSH/LH, Testosterone, DHT, Estrogen

63
Q

Why would androgen insensitivity syndrome produce no internal male or female genitalia?

A

Testosterone has no effect to produce male genitalia

Mullerian inhibiting hormone gets rid of internal female genitalia

64
Q

Androgens refer to what 2 molecules?

A

Testosterone and DHT

65
Q

What are the hormone levels in 5-alpha-reductase deficiency?

A

Normal everything.

*internal genitalia male, external female until puberty

66
Q

What causes gynecomastia (excess breast tissue in males)?

A

excess Estrogen
(E/T ration high)

*common in aging

67
Q

What condition includes the following: tall, epiphyses not closed, osteoporosis, normal genitalia, and abnormal semen?

A 
No aromatase (so no estrogen) 
No estrogen receptors
68
Q

Why would a continuous GnRH treatment be appropriate for prostate cancer?

A

GnRH that NOT in pulses down-regulates FSH and LH receptors

also, 5-alpha reductase inhibitors (no DHT) is a treatment for prostate cancer

69
Q

What developmental indicators are affected by hormones?

A

height

length at birth, bone growth

70
Q

Is brain size (head circumference) affected by hormones?

A

NO

*genetics, nutrition, environment

71
Q

What 3 hormones affect length before birth?

A

insulin
IGF-1
IGF-2

72
Q

T/F

Endocrine causes of childhood obesity is common

A

False

0.1%

73
Q

T/F

Height after birth isn’t affected by hormones

A

FALSE

*GH and IGF-1

74
Q

Describe the growth feedback loop

A

GHRH > GH > IGF-1

75
Q

What does thyroid hormone do developmentally?

A

Height (acts in concert with GH)

Full fetal/child brain development

76
Q

What are the 4 main hormones for growth?

A

GH
IGF-1
Thyroid hormone
Estrogen/testosterone (added at puberty)

*remember - estrogen closes epiphyses

77
Q

What are some endocrine causes of short stature?

A

hypothyroidism
abnormal GH secretion
excess Cortisol
Precocious puberty

78
Q

Thyroid hormone and GH both affect ____ more than _____.

A

height

weight

79
Q

What effect does GH deficiency have on teeth?

A

gaps

small mandible

80
Q

What does GH excess cause?

A

Gigantism or acromegaly

81
Q

What is the difference between central and peripheral precocious puberty?

A

early puberty brought on by increases GnRH in Central

brought on by abnormal hormone source in Peripheral

82
Q

How is central precocious puberty treated?

peripheral?

A

continuous GnRH

treat underlying cause

83
Q

T/F

Hypothyroidism and GH deficiency can present similarly.

A

True

*fatigue, no growth in height, slow pulse, delayed deep tendon relaxation

Tim's Cards (140 decks)

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